Shan-Shan Wang1, Ya-Guang Wang2, Hai-Ying Chen3, Zhi-Ping Wu3, Heng-Ge Xie1. 1. Neurology Department of Nanlou Clinical Division, Chinese PLA General Hospital, Fuxing Road 28, Beijing 100853, China. jessicass33@gmail.com; xiehengge@163.com. 2. Academy of Chinese Military Medicine Science, Beijing 100850, China. 3. Neurology Department of Nanlou Clinical Division, Chinese PLA General Hospital, Fuxing Road 28, Beijing 100853, China.
Abstract
OBJECTIVES: To establish a rat model of post-stroke depression (PSD), and examine expression of genes encoding corticotropin releasing factor (CRF), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) in the hypothalamus of PSD rats. METHODS: Rats were subjected to middle cerebral artery occlusion (MCAO) and chronic mild unpredictable stress (CUMS). Open field test and sucrose preference were used to examine depressive-like behaviors. Observed changes in gene expression levels in the hypothalamus of PSD rats were evaluated. RESULTS: MCAO with CUMS resulted in reduction of sucrose preference and locomotor activity. Genes encoding TNF-α, IL-1β and CRF were highly expressed in the hypothalamus of rats subjected to MCAO and CUMS. The antidepressant citalopram, a selective serotonin reuptake inhibitor, had inhibitory effects on the expression of the aforementioned genes. We observed a correlation between CRF and IL-1β mRNA levels in the citalopram-treated group of rats. CONCLUSION: The etiology of PSD is associated with cytokine expression in the hypothalamus and with hypothalamic-pituitary-adrenal axis activity. Citalopram administration inhibited the expression of TNF-α and IL-1β transcripts in the hypothalamus, suggesting that selective serotonin reuptake inhibitors may be appropriate for PSD therapy.
OBJECTIVES: To establish a rat model of post-stroke depression (PSD), and examine expression of genes encoding corticotropin releasing factor (CRF), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) in the hypothalamus of PSD rats. METHODS:Rats were subjected to middle cerebral artery occlusion (MCAO) and chronic mild unpredictable stress (CUMS). Open field test and sucrose preference were used to examine depressive-like behaviors. Observed changes in gene expression levels in the hypothalamus of PSD rats were evaluated. RESULTS:MCAO with CUMS resulted in reduction of sucrose preference and locomotor activity. Genes encoding TNF-α, IL-1β and CRF were highly expressed in the hypothalamus of rats subjected to MCAO and CUMS. The antidepressant citalopram, a selective serotonin reuptake inhibitor, had inhibitory effects on the expression of the aforementioned genes. We observed a correlation between CRF and IL-1β mRNA levels in the citalopram-treated group of rats. CONCLUSION: The etiology of PSD is associated with cytokine expression in the hypothalamus and with hypothalamic-pituitary-adrenal axis activity. Citalopram administration inhibited the expression of TNF-α and IL-1β transcripts in the hypothalamus, suggesting that selective serotonin reuptake inhibitors may be appropriate for PSD therapy.